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    Dual RNAseq shows the human mucosal immunity protein, MUC13, is a hallmark of Plasmodium exoerythrocytic infection

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    Type
    Preprint
    Authors
    LaMonte, Gregory
    Orjuela-Sanchez, Pamela
    Wang, Lawrence
    Li, Shangzhong
    Swann, Justine
    Cowell, Annie
    Zou, Bing Yu
    Abdel-Haleem, Alyaa M. cc
    Villa-Galarce, Zaira
    Moreno, Marta
    Tong-Rios, Carlos
    Vinetz, Joseph
    Lewis, Nathan
    Winzeler, Elizabeth A
    KAUST Department
    Biological and Environmental Sciences and Engineering (BESE) Division
    Bioscience Program
    Computational Bioscience Research Center (CBRC)
    Date
    2017-10-03
    Permanent link to this record
    http://hdl.handle.net/10754/625854
    
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    Abstract
    The exoerythrocytic stage of Plasmodium malaria infection is a critical window for prophylactic intervention. Using a genome-wide dual RNA sequencing of flow-sorted infected and uninfected hepatoma cells we identify the human mucosal immunity gene, Mucin13 (MUC13), as strongly upregulated during Plasmodium exoerythrocytic hepatic-stage infection. We confirm that MUC13 expression is upregulated in hepatoma cell lines and primary hepatocytes. In immunofluorescence assays, host MUC13 protein expression distinguishes infected cells from adjacent uninfected cells and shows similar colocalization with parasite biomarkers such as UIS4 and HSP70. We further show that localization patterns are species independent, distinguishing both P. berghei and P. vivax infected cells, and that MUC13 can be used to identify compounds that inhibit parasite replication in hepatocytes across all Human-infecting Plasmodium species. This data presents a novel interface of host-parasite interactions in Plasmodium, in that a component of host mucosal immunity is reprogrammed to assist the progression of infection.
    Citation
    LaMonte G, Orjuela-Sanchez P, Wang L, Li S, Swann J, et al. (2017) Dual RNAseq shows the human mucosal immunity protein, MUC13, is a hallmark of Plasmodium exoerythrocytic infection. Available: http://dx.doi.org/10.1101/183764.
    Sponsors
    We thank the members of the Winzeler and Lewis labs for advice and critical reading of the manuscript. In addition, we thank Medicines for Malaria Venture for all of their support of the insectary in Peru. We would also like to thank the UCSD Institute for Genomic Medicine Sequencing Core Facility and the UCSD Human Embryonic Stem Cell Flow Cytometry Core Facility for their technical support. G.L. is supported by an A.P. Giannini Post-Doctoral Fellowship. E.A.W. is supported by grants from the NIH (5R01AI090141 and R01AI103058). N.E.L. and S.L received funding from the NIGMS (R35 GM119850) and the Novo Nordisk Foundation through the Center for Biosustainability at the Technical University of Denmark (NNF10CC1016517). The P. vivax work was supported by grants to J.M.V from the NIH (D43TW007120 and U19AI089681). A.N.C received support from a NIH T32 AI 007036 training grant.
    Publisher
    Cold Spring Harbor Laboratory
    DOI
    10.1101/183764
    Additional Links
    https://www.biorxiv.org/content/early/2017/10/02/183764
    ae974a485f413a2113503eed53cd6c53
    10.1101/183764
    Scopus Count
    Collections
    Biological and Environmental Sciences and Engineering (BESE) Division; Preprints; Bioscience Program; Computational Bioscience Research Center (CBRC)

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